Biology and markers of preeclampsia

Preeclampsia is a syndrome specific of pregnancy and placenta diagnosed after 20 WG on the association of an hypertension and a proteinuria. It is responsible for significant maternal-fetal morbidity and mortality which justify the development of markers for screening, diagnosis and prognosis. These markers are actors or witnesses to the various stages and mechanisms of the disease : the initial defect of trophoblast invasion and remodeling of uterine arteries (proteases [PAPP-A, ADAM-12, uPA, MMPs], their inhibitors, and angiogenic factors [PlGF, sflt-1, s-eng]) which induces hydrostatic abnormalities (uterine doppler) and placental hypoperfusion with dysoxia (HIF-1 alpha) and oxidative stress (free radicals, peroxynitrites, oxidized LDL). This results in impaired placental functions including endocrine and metabolic functions (hCG, leptin) with increase in placental apoptosis and necrosis with the release of exosomes and toxic placental fragments (STBM) and their content (RNA, DNA and proteins). This fragments amplify the gestational inflammation (IL6, TNF alpha; activation of leukocytes and macrophages [elastase, neopterin] and complement) and lead to a deterioration of the maternal endothelium (vasoconstriction [ET2, TxA2]; platelet adhesion [sVCAM - 1 alpha), aggregation and activation; impaired vascular permeability) generating edema, hypertension, atherosclerosis and glomerular nephropathy (proteinuria, hyperuricemia). Other markers such as PP13 and PTX3 seem of interest even if their functions are poorly understood. Preeclampsia develops on a predisposed maternal environment (genetic, epigenetic infectious, and endocrine factors) characterized by a maternal inadequacy to pregnancy.